Neurophysiological Effects Induced in the Nervous Tissue by Low-Frequency, Pulsed Magnetic Fields

Summary The influence of pulsed magnetic fields (PMF) on the properties of nervous tissue was investigated. Hippocampal slices or synaptosomes obtained from hippocampal tissue were used as model systems. The amplitude of potentials recorded in vitro from one of the hippocampal pathways (Schaffer collaterals that use glutamate as a neurotransmitter) was employed as a measure of the influence of magnetic fields on synaptic efficiency. The synaptic glutamate turnover and radioactive calcium accumulation were used as markers of the PMF influence on biochemistry of synaptic mechanisms. The exposure of hippocampal slices for 30 min to PMF amplified evoked potentials. While the frequency of 0.16 Hz exerted the strongest effect, lower (0.01, 0.07, 0.03 Hz) and higher (0.5 Hz) frequencies were much less effective. The enhancement of the neuronal excitability was correlated with significant increase in the neuronal spontaneous activity mediated by electrical synapses. The PMF-induced changes in the excitability of the tissue were accompanied by an increase in the synaptic turnover of glutamate. The release of radioactive D-Aspartate (a glutamate analog used as a marker for glutamate turnover) from the slices, and its uptake by synaptosomes were enhanced, and reduced respectively, following the stimulation with pulsed magnetic fields. The frequency which was the most efficient in amplification of evoked potentials (0.16 Hz) was also the most effective in the modulation of the release and uptake processes. The PMF-induced changes in neurotransmitter turnover coincided with an increase in ⁴⁵Ca²⁺ accumulation observed in hippocampal slices exposed to PMF.     

孕哺期全氟辛烷磺酸染毒对大鼠海马细胞钙稳态的影响

为了阐明孕哺期全氟辛烷磺酸(perfluorooctane sulfonate,PFOS)染毒对大鼠及其仔鼠海马细胞钙稳态的影响,将妊娠Wistar大鼠30只,从妊娠第1天开始对实验组分别以72 mg·kg-1(low,L)、14.4 mg·kg-1(high,H)(以饲料中的PFOS计)的PFOS进行染毒至仔鼠生后3...     

邻苯二甲酸二丁酯诱导小鼠神经行为学改变及相关生理生化指标分析

探究邻苯二甲酸二丁酯诱导小鼠神经行为学改变及与细胞外调节蛋白激酶(ERK1/2)通路相关蛋白的关联.雄性KM小鼠36只,随机分成4组:生理盐水组、50 mg·kg~(-1)·d~(-1) DBP组、50 mg·kg~(-1)·d~(-1)维生素E(VE)组、DBP+VE组,连续灌胃处理28 d,观察Morris水迷宫结果,检测小鼠脑海马组织的氧化应激(活性氧(ROS)荧光强度、还原型谷胱甘肽(GSH)与丙二醛(MDA)含量)、脑源性神经营养因子(BDNF)、磷酸化cAMP反应元件结合蛋白(p-CREB)、caspase-3水平,Western blot分析ERK1/2及其磷酸化(p-ERK1/2)水平;HE、Nissl染色及Hoechst 33258荧光染色分析脑组织CA1区病理学变化.结果表明,与对照组比较,50 mg·kg~(-1)·d~(-1) DBP组小鼠的学习记忆下降,氧化应激、p-ERK1/2、caspase-3水平上升,BDNF、p-CREB表达下降,差异均有统计学意义(p0.05,p0.01);海马组织CA1病理学损伤及凋亡程度增加.给予抗氧化剂VE处理后,DBP+VE组小鼠的学习记忆上升,氧化应激、p-ERK1/2、caspase-3水平降低,BDNF、p-CREB表达上升,差异均有统计学意义(p0.05);海马组织CA1病理学损伤及凋亡程度降低.由此推测,DBP暴露导致小鼠海马组织CA1病理学损伤、神经元凋亡程度增加、学习记忆下降、其神经行为学改变可以通过添加VE得到缓解,相关生理生化指标测试表明ERK系统应激氧化性损伤机制参与介导了毒理学过程.     

邻苯二甲酸二丁酯影响阿尔茨海默病大鼠学习记忆能力的分子机制研究

为探究邻苯二甲酸二丁酯（DBP）影响阿尔茨海默病（AD）大鼠学习记忆能力的分子机制,将56只SPF级5~6周龄雌性Wistar大鼠随机平均分为7组：阴性对照组、0.25 mg·kg^-1·d^-1 DBP组、2.5 mg·kg^-1·d^-1 DBP组、25 mg·kg^-1·d^-1 DBP组、250 mg·kg^-1·d^-1 DBP组、AD模型组和AD+25 mg·kg^-1·d^-1 DBP组.连续灌胃处理28 d,观察Morris水迷宫结果,检测脑海马组织中活性氧（ROS）、还原型谷胱甘肽（GSH）、丙二醛（MDA）、8-羟基脱氧鸟苷（8-OHdG）的含量;采用实时荧光定量PCR （qPCR）检测Bcl-2、Bax和Caspase-3 mRNA的转录水平;通过免疫印迹试验（Western blot）检测Bcl-2、Bax和Caspase-3的蛋白表达水平.结果表明,与阴性对照组相比,不同染毒组、DBP组大鼠的学习记忆能力下降,氧化应激水平上升,且随DBP染毒浓度升高而加剧（p<0.05,p<0.01）;AD+25 mg·kg^-1·d^-1 DBP组较AD模型组大鼠的学习记忆能力损伤加剧,氧化应激水平和Bcl-2/Bax/Caspase-3信号通路上调,差异具有统计学意义（p<0.05）.由此推测,DBP可通过氧化应激作用,上调Bcl-2/Bax/Caspase-3信号通路,加剧AD大鼠海马组织的损伤,导致学习记忆能力下降.本文通过DBP影响AD大鼠学习记忆能力的分子机制研究,揭示了氧化应激对凋亡信号通路的作用,并为进一步研究DBP的毒性提供了理论和数据依据.     

内质网应激介导的凋亡在PBDE-47致大鼠海马损伤中的作用

为了明确内质网应激(endoplasmic reticulum stress,ERS)介导的凋亡在2,2’,4,4’-四溴联苯醚(2,2’,4,4’-tetrabromodiphenylether,PBDE-47)致大鼠神经毒性中的作用,在脑发育的突增期(出生第10天),分别用0 mg·kg~(-1)、1 mg·kg~(-1)、5 mg·kg~(-1)和10mg·kg~(-1)PBDE-47进行单次灌胃染毒,并从出生第8天开始每天给予150 mg·kg~(-1)ERS抑制剂4-苯基丁酸(phenylbutyric acid,PBA),持续3周。仔鼠出生第8周末,从对照组、10 mg·kg~(-1)PBDE-47处理组、150 mg·kg~(-1)PBA处理组和150 mg·kg~(-1)PBA+10mg·kg~(-1)PBDE处理组中随机选取8只大鼠进行水迷宫实验。然后将所有动物断头处死,分离大鼠海马组织,观察其海马组织形态学改变、测定ERS标志分子(GRP78、IRE1和CHOP)和凋亡相关蛋白Cyt c的表达水平。结果显示,10 mg·kg~(-1)PBDE-47处理可导致雌性大鼠海马CA4区细胞排列紊乱、锥形神经细胞数量减少甚至消失,尼氏小体数量减少,大鼠逃避潜伏期延长(P0.05)。5和10 mg·kg~(-1)PBDE-47处理可显著上调ERS相关蛋白IRE1和CHOP的表达水平(P0.05),并明显增强海马组织凋亡相关蛋白Cyt c的表达。PBA干预可明显降低PBDE-47诱导的IRE1和CHOP以及Cyt c蛋白的表达水平,提示PBDE-47可通过ERS介导凋亡,导致大鼠海马组织损伤,从而影响大鼠学习记忆功能。     

全氟辛酸对大鼠海马细胞内钙离子浓度的影响

采用连续灌胃染毒的方法,探讨了全氟辛酸(Perfluorooctanoic acid,PFOA)经口急性染毒对大鼠海马细胞内钙离子浓度的影响.选择雄性Wistar大鼠40只,实验组PFOA染毒剂量分别为2、8、30mg·kg-1(bw).连续灌胃染毒7天后,制备海马单细胞悬液,采用Fura-2/AM荧光探针法测定海马细胞内游离钙离子浓度([Ca2+]i),使用固相萃取-高效液相色谱/质谱联机法(HPLC/MS-MIS)检测血清与脑组织中PFOA浓度.结果表明,染毒组大鼠血清与脑中PFOA浓度均显著高于对照组水平(p<0.01),血清与脑中PFOA浓度之间存在显著的正相关关系(r2=0.611,p<0.01).PFOA染毒8、30mg·kg-1(bw)实验组海马细胞[Ca2+]i分别为(207.89±22.84)nmol·L-1和(284.19±14.75)nmol·L-1,显著高于对照组((141.68±11.47)nmol·L-1)和PFOA染毒2mg·kg-1(bw)实验组((147.38±19.23)nmol·L-1)(p<0.01).大鼠脑、血清中PFOA浓度分别与海马[Ca2+]i存在正相关关系(r2=0.552,p<0.01;r2=0.756,p<0.01).研究结果显示,PFOA暴露可使血清和脑组织中PFOA浓度增加,引起大鼠海马神经元细胞[Ca2+]i升高.     

Survival Under Conditions of Environmental Stress: Variability of Brain Morphology and Behavior in the House Mouse

Two populations of laboratory mice lived outdoors in open pens for two years. Thereafter, some of them were bred in the laboratory. Morphometric analysis showed that the size of the synaptic projection area of mossy fibers (in the CA3 region of the hippocampus), which has an important functional role, and some behavioral traits of the open-pen mouse progeny had significant genetically determined differences from those in the initial population. This was attributed to differential breeding accounted for by the influence of severe environmental factors. Under environmental stress, selection occurred in the population and the mice with behavioral and neuromorphological characteristics differing from those of the control group proved to be better adapted to such conditions.     

Neurobiology of the homing pigeon—a review

Homing pigeons are well known as good homers, and the knowledge of principal parameters determining their homing behaviour and the neurological basis for this have been elucidated in the last decades. Several orientation mechanisms and parameters—sun compass, earth’s magnetic field, olfactory cues, visual cues—are known to be involved in homing behaviour, whereas there are still controversial discussions about their detailed function and their importance. This paper attempts to review and summarise the present knowledge about pigeon homing by describing the known orientation mechanisms and factors, including their pros and cons. Additionally, behavioural features like motivation, experience, and track preferences are discussed. All behaviour has its origin in the brain and the neuronal basis of homing and the neuroanatomical particularities of homing pigeons are a main topic of this review. Homing pigeons have larger brains in comparison to other non-homing pigeon breeds and particularly show increased size of the hippocampus. This underlines our hypothesis that there is a relationship between hippocampus size and spatial ability. The role of the hippocampus in homing and its plasticity in response to navigational experience are discussed in support of this hypothesis.     

The effect of chronic formaldehyde exposure on the hippocampus in chronic cerebral hypoperfusion rat model

The aim of this study was to evaluate the effect of chronic formaldehyde (FA) exposure on the hippocampus in the chronic cerebral hypoperfusion rat model. Seventy-two male Sprague-Dawley rats were randomly divided into four groups: (A) sham-operated bilateral common carotid artery occlusion (BCCAO) with room air inhalation, (B) BCCAO with room air inhalation, (C) sham-operated BCCAO with FA inhalation at a concentration of 10?mL?vapor?m^?3, 1?h per day for 90 days, and (D) BCCAO with FA inhalation. Decreased mobility, injected conjunctivae, and overreaction were observed in groups C and D rats after 30 days of FA exposure. The level of malondialdehyde (MDA) increased significantly in group D at 90 days after FA exposure. The expression of Bax protein increased, while Bcl-2 and NR2B proteins decreased significantly in group D compared to group B or C. Neuronal nuclear antigen (NeuN) positive cells decreased significantly in group D. Neuronal loss, oxidative stress, and the expression of proteins were more prominent at 90 days after FA exposure, especially in group D. Oxidative stress-induced neuronal damages in the hippocampus may be a possible mechanism of neurotoxicity as a result of chronic FA exposure. Chronic exposure of FA caused more neuronal damage in the chronic cerebral hypoperfusion rat model.     

氯化甲基汞对大鼠海马c-jun蛋白表达的影响

为了探讨氯化甲基汞(MMC)对大鼠海马损伤的分子机制,应用免疫组织化学方法观察了氯化甲基汞对大鼠海马JUN蛋白表达的影响(对照组为0.9%生理盐水、暴露组浓度分别为0.05,0.5,5mg/kg;取样时间分别为20,60,240,1440min).结果发现,暴露组大鼠海马JUN蛋白表达均高于对照组,氯化甲基汞对大鼠海马JUN蛋白表达与其浓度之间有一定的剂量反应关系,表明即刻早期基因(c-jun)参与了氯化甲基汞对海马损害的毒性过程.